Adenosine reduces GABAergic IPSC frequency via presynaptic A1 receptors in hypothalamic paraventricular neurons projecting to rostral ventrolateral medulla

Tae Hee Han,Soo Hwa Jang,So Yeong Lee,Pan Dong Ryu. Neuroscience Letters

Volume 490, Issue 1, 18 February 2011, Pages 63–67. doi:10.1016/j.neulet.2010. 12.026. The paraventricular nucleus (PVN) is a brain region that has projections that go to RVLM and down to the IML in order to modulate sympathetic outflow. The purpose of this study was to determine whether adenosine was was playing a role in modulating gaba release from PVN-RVLM neurons. Using young male Sprague-Dawley they labelled PVN-RVLM neurons by injecting Fluospheres- Red into the RVLM and they allowed the animal to recover for 5-7 days. the brain was sectioned and the labelled PVN neurons were selected for recording. In response to adenosine, they saw inhibitory postsynaptic currents . When compared to the before activity there was a decrease in firing but not in amplitude and the response was concentration dependent. Then they used antagonist to A 1 receptor and the A2  receptor  and saw that there was no change in the firing of the neuron. however, when adenosine was given  after the  microinjection of the A1 antagonist they found that the iPSCs was inhibited.  the microinjection of  the A2 antagonist  did not prevent the IPSCs that occur in response to  adenosine injection. These data demonstrate that adenosine is playing a  role presynaptically  in attenuating GABA release and this mediated by adenosine acting on A1 receptors. -MD

Acute intermittent optogenetic stimulation of nucleus tractus solitarius neurons induces sympathetic long-term facilitation.

Yamamoto K, Lalley PM, Mifflin SW.

Am J Physiol Regul Integr Comp Physiol. 2014 Dec 17:ajpregu.00381.2014

                In this paper, they built on previous work that showed that the effect of acute intermittent hypoxia (AIH) on long term facilitation (LTF) of phrenic nerve activity (PNA) and renal sympathetic nerve activity (RSNA) seems to be routed through the nucleus tractus solitarius (NTS), and that you could induce the same effect by electrical stimulation of the carotid sinus, even without hypoxia. They took this idea a step further by causing expression of channelrhodopsin in the caudal NTS, via a virus that would cause preferential expression in glutamatergic neurons.

                Once they had this system in operation, they compared the effects of AIH with the effects of acute intermittent optogenetic stimulation (AIO) on RSNA and PNA immediately after, and 60 minutes after periods of stimuli. They found that AIO in the caudal NTS produces a similar, but weaker, response to that seen after AIH (RSNA and PNA increased by 60% and 100% after AIO, but by 80 and 130% after AIH).  They also found that, while both stimuli increased the power spectral density of RSNA and PNA at their own primary frequencies, neither stimulus was able to increase synchronization of PNA with RSNA. -DH